text: Because the glycocalyx is so prominent throughout the cardiovascular system, disruption to this structure has detrimental effects that can cause disease. Certain stimuli that cause atheroma may lead to enhanced sensitivity of vasculature. Initial dysfunction of the glycocalyx can be caused by hyperglycemia or oxidized low-density lipoproteins (LDLs), which then causes atherothrombosis. In microvasculature, dysfunction of the glycocalyx leads to internal fluid imbalance, and potentially edema. In arterial vascular tissue, glycocalyx disruption causes inflammation and atherothrombosis.
  Experiments have been performed to test precisely how the glycocalyx can be altered or damaged.  One particular study used an isolated perfused heart model designed to facilitate detection of the state of the vascular barrier portion, and sought to cause insult-induced shedding of the glycocalyx to ascertain the cause-and-effect relationship between glycocalyx shedding and vascular permeability.  Hypoxic perfusion of the glycocalyx was thought to be sufficient to initiate a degradation mechanism of the endothelial barrier.  The study found that flow of oxygen throughout the blood vessels did not have to be completely absent (ischemic hypoxia), but that minimal levels of oxygen were sufficient to cause the degradation.  Shedding of the glycocalyx can be triggered by inflammatory stimuli, such as tumor necrosis factor-alpha.  Whatever the stimulus is, however, shedding of the glycocalyx leads to a drastic increase in vascular permeability.  Vascular walls being permeable is disadvantageous, since that would enable passage of some macromolecules or other harmful antigens.
  Other sources of damage to the endothelial glycocalyx have been observed in several pathological conditions such as inflammation, hyperglycemia, ischemia-reperfusion,  viral infections and sepsis.
  Some key components of the glycocalyx such as syndecans, heparan sulphate, chondroitin sulphate and hyaluronan can be shed of the endothelial layer by enzymes. Hyaluronidase, hepararanse/heparinase, matrix and membrane-type matrix metalloproteases, thrombin, plasmin and elastase are some examples of enzymes that can induce shedding of the glycocalyx and these sheddases can therefor contribute to degradation of the glycocalyx layer in several pathological conditions. Research shows that plasma hyaluronidase activity is decreased in experimental as well as in clinical septic shock and is therefore not considered to be a sheddase in sepsis. Concomitant, the endogenous plasma inhibition of hyaluronidase is increased and could serve as a protection against glycocalyx shedding.
  Fluid shear stress is also a potential problem if the glycocalyx is degraded for any reason.  This type of frictional stress is caused by the movement of viscous fluid (i.e. blood) along the lumen boundary. Another similar experiment was carried out to determine what kinds of stimuli cause fluid shear stress. The initial measurement was taken with intravital microscopy, which showed a slow-moving plasma layer, the glycocalyx, of 1 μm thick.  Light dye damaged the glycocalyx minimally, but that small change increased capillary hematocrit. Thus, fluorescence light microscopy should not be used to study the glycocalyx because that particular method uses a dye. The glycocalyx can also be reduced in thickness when treated with oxidized LDL. These stimuli, along with many other factors, can cause damage to the delicate glycocalyx.  These studies are evidence that the glycocalyx plays a crucial role in cardiovascular system health.